Functional links have been found between the brain, endocrine and immune system as referenced in Mocchegiani et al. (Thyroid and thymic endocrine function and survival in severely traumatized patients with or without head injury, Intensive Care Med, 1995, 21:334-341), incorporated herein in its entirety by reference. The general consensus is that there is a presence of strongly reduced thyroid hormone serum levels in head trauma. Further, following severe head trauma, specific immunity, particularly T-cell mediated immunity is found to be altered in that there is a decreased ratio of T-helper/T-suppressor cells, reduced mitogen responsiveness and impaired cutaneous delayed hypersensitivity.
Mocchegiani et al. suggested involvement of the thymic function in the depressed immunity of patients having head trauma. They determined the blood concentration of thymulin in head trauma injured patients and compared this result with that found in patients without head trauma. These values were correlated with thyroid hormone concentrations and the impact that the thymic hormone measurements have for predicting overall survival of the patient. Blood samples were taken from the patients within 24 hours after admission and then again 5 and 10 days later. Mocchegiani found that thymic endocrine activity as measured by the level of thymulin, a thymic peptide, is reduced in those patients having a head injury as compared to patients without a head injury. Mocchegiani also found that this reduction of thymic endocrine activity is correlated with the depth of coma, i.e. the clinical indication of the severity of brain damage. Mocchegiani postulates that the low thymulin levels of the patients suffering from head injury may be due to a reduced production of this peptide by the thymus. All of the studies of Mocchegiani involved adults having head injury.
Traumatic brain injury (TBI) is broadly defined as damage to the brain as a result of physical force which may cause alteration of normal brain processes due to changes in the brain structure or function. A closed head traumatic brain injury can be caused by a rapid movement of the head which causes the brain to essentially bounce off the inside of the skull. A closed head TBI may be the result of a motor vehicle accident, a fall, or forceful shaking as in Shaken Baby Syndrome. Shaken Baby Syndrome is defined as one or more of a group of symptoms (as limb paralysis, epilepsy, vision loss, or mental retardation) that tend to occur in an infant which has been severely shaken but that may also result from other actions (as tossing) causing internal trauma (as hemorrhage, hematoma, or contusions) especially to the brain region, and that may ultimately result in the death of the infant. Determining the cause of death of an infant can be a very difficult task especially as it relates to sudden infant death syndrome (SIDS) or shaken baby syndrome.
As illustrated above, a great deal of work has been devoted to the impact of head trauma and brain function on the immune system, however there has not been an examination of the effect of head trauma on the thymus, the site of maturation and negative selection of T-cells, and the source of circulating T-cells. What is needed is a quantitative assessment of post-mortem thymus integrity. Thymus integrity in children could reflect manner of death. Less integrity is correlated with more traumatic death. Thus, a more universal (quantitative, standardized) process for assessing post-mortem thymus integrity could aid in determining manner of infant or child death.